Q-omics provides the consensus-scored NCALD profile across patient tissues and cancer cell-line models. NCALD expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, NCALD is differentially expressed in 12, with the highest sampling consensus in BLCA. Additionally, NCALD protein abundance shows 24,664 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, BLCA, and GBM as cancer lineages where NCALD shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for NCALD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NCALD survival associations across molecular data types. NCALD RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NCALD RNA expression–survival associations across cancer types. High NCALD expression shows unfavorable associations in BLCA, UVM and LAML, but favorable associations in KIRC, HNSC and LUAD. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for NCALD RNA expression.
This table summarizes NCALD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 6. The strongest signals are observed in LUAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for NCALD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NCALD shows lower tumor expression in BLCA, LUAD, LUSC and BRCA and higher tumor expression in KIRC and KICH. The BLCA box plot shows higher NCALD RNA expression in normal versus tumor tissue (log2 FC = −3.307, t-test p < 0.001).
This table shows molecular features associated with NCALD in patient tissues and cancer cell lines. In patient samples, NCALD shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, NCALD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Lymphoma.
